Coronary Artery Anatomy

The major vessels of the coronary circulation are the left main coronary that
divides into left anterior descending (LAD) and circumflex branches, and the
right main coronary artery. The left and right coronary arteries originate
at the base of the aorta from openings called the coronary ostia located behind
the aortic valve leaflets.
The left and right coronary arteries and their branches lie on the surface of the
heart, and therefore are sometimes referred to as the epicardial coronary
vessels. These vessels distribute blood flow to different regions of the heart
muscle. When the vessels are not diseased, they have a low vascular
resistance relative to their more distal and smaller branches that comprise
the microvascular network. As in all vascular beds, it is the small arteries and
arterioles in the microcirculation that are the primary sites of vascular resistance,
and therefore the primary site for regulation of blood flow. The arterioles branch
into numerous capillaries that lie adjacent to the cardiac myocytes. A high
capillary-to-cardiomyocyte ratio and short diffusion distances ensure adequate
oxygen delivery to the myocytes and removal of metabolic waste products from
the cells (e.g., CO2 and H+). Capillary blood flow enters venules that join together
to form cardiac veins that drain into the coronary sinus located on the posterior
side of the heart, which drains into the right atrium. There are also anterior
cardiac veins and thesbesian veins (the smallest cardiac veins drain
into all 4 chambers) drain directly into the right atrium chamber.
Although there is considerable heterogeneity among people, the following table
indicates the regions of the heart that are generally supplied by the different
coronary arteries. This anatomic distribution is important because these cardiac
regions are assessed by 12-lead ECGs to help localize ischemic or infarcted
regions, which can be loosely correlated with specific coronary vessels; however,
because of vessel heterogeneity, actual vessel involvement in ischemic
conditions needs to be verified by coronary angiograms or other imaging
techniques.

Anatomic
Region of
Heart

Coronary Artery
(most likely
associated)

Inferior

Right coronary

Anteroseptal

Left anterior descending

Anteroapical

Left anterior descending

(distal)

Anterolateral

Circumflex

Posterior

Right coronary artery

The following summarizes important features of coronary blood flow:

Flow is tightly coupled to oxygen demand. This is necessary because the

heart has a very high basal oxygen consumption (8-10 ml O2/min/100g)
and the highest A-VO2 difference [the difference in the oxygen content
of the blood between the arterial blood and the venous blood] of a major
organ (10-13 ml/100 ml). In non-diseased coronary vessels, whenever
cardiac activity and oxygen consumption increases, there is an increase in
coronary blood flow (active hyperaemia) that is nearly proportionate to the
increase in oxygen consumption.

Good autoregulation between 60 and 200 mmHg perfusion pressure helps

to maintain normal coronary blood flow whenever coronary perfusion
pressure changes due to changes in aortic pressure.

Adenosine is an important mediator of active hyperaemia and

autoregulation. It serves as a metabolic coupler between oxygen
consumption and coronary blood flow. Nitric oxide is also an important
regulator of coronary blood flow.

Activation of sympathetic nerves innervating the coronary vasculature

causes only transient vasoconstriction mediated by 1-adrenoceptors.
This brief (and small) vasoconstrictor response is followed by vasodilation
caused by enhanced production of vasodilator metabolites (active
hyperaemia) due to increased mechanical and metabolic activity of the
heart resulting from 1-adrenoceptor activation of the myocardium.
Therefore, sympathetic activation to the heart results in coronary
vasodilation and increased coronary flow due to increased metabolic
activity (increased heart rate, contractility) despite direct vasoconstrictor
effects of sympathetic activation on the coronaries. This is termed
"functional sympatholysis."

Parasympathetic stimulation of the heart (i.e., vagal nerve activation)

elicits modest coronary vasodilation (due to the direct effects of released
acetylcholine on the coronaries). However, if parasympathetic activation
of the heart results in a significant decrease in myocardial oxygen
demand due to a reduction in heart rate, then intrinsic metabolic
mechanisms will increase coronary vascular resistance by constricting the
vessels.

Progressive ischemic coronary artery disease results in the growth of new

vessels (termed angiogenesis) and collateralization within the
myocardium. Collateralization increases myocardial blood supply by
increasing the number of parallel vessels, thereby reducing vascular
resistance within the myocardium.

Extravascular compression (compression of the coronary arteries) during

systole markedly affects coronary flow; therefore, most of the coronary
flow occurs during diastole. Because of extravascular compression, the
endocardium is more susceptible to ischemia especially at lower perfusion
pressures. Furthermore, with tachycardia there is relatively less time
available for coronary flow during diastole to occur this is particularly
significant in patients with coronary artery disease where coronary flow
reserve (maximal flow capacity) is reduced.

In the presence of coronary artery disease, coronary blood flow may be reduced.
This will increase oxygen extraction from the coronary blood and decrease the
venous oxygen content. This leads to tissue hypoxia and angina. If the lack of
blood flow is due to a fixed stenotic lesion in the coronary artery (because of
atherosclerosis), blood flow can be improved within that vessel by:

Placing a stent within the vessel to expand the lumen

Using an intracoronary angioplasty balloon to stretch the vessel
open
Bypassing the diseased vessel with a vascular graft.

If the insufficient blood flow is caused by a

blood clot (thrombosis), a thrombolytic
drug that dissolves clots may be
administered. Anti-platelet drugs and
aspirin are commonly used to prevent the
reoccurrence of clots. If the reduced flow is
due to coronary vasospasm, then coronary
vasodilators can be given
(e.g., nitrodilators, calcium-channel
blockers) to reverse and prevent
vasospasm.

Coronary Veins
The coronary sinus is a collection of veins joined together to form a large
vessel that collects blood from the heart muscle (myocardium). It delivers
deoxygenated blood to the right atrium, as do the superior and inferior vena
cava.

The coronary sinus opens into the right atrium, at the coronary sinus orifice,
between the inferior vena cava and the right atrioventricular orifice. It returns
the blood from the substance of the heart, and is protected by a semicircular fold
of the lining membrane of the auricle, the valve of coronary sinus (or valve of
Thebesius). The sinus, before entering the auricle, is considerably dilated - nearly
to the size of the end of the little finger. Its wall is partly muscular, and at its
junction with the great cardiac vein is somewhat constricted and furnished with a
valve consisting of two unequal segments.
The coronary sinus receives blood mainly from
the small, middle, great and oblique cardiac veins. It also receives blood from
the left marginal vein and the left posterior ventricular vein. The anterior cardiac
veins do not drain into the coronary sinus but drain directly into the right atrium.
The Great Cardiac Vein (left coronary vein) begins at the apex of the
heart and ascends along the anterior longitudinal sulcus to the base of the
ventricles. It then curves to the left in the coronary sulcus, and reaching the back
of the heart, opens into the left extremity of the coronary sinus.